Autophagy is a conserved cellular process that is activated under conditions of nutrient stress to promote cell survival. The induction of autophagy in the heart, liver and diaphragms of mammals in the perinatal period is an essential adaptation that is required to survive early neonatal starvation. Constitutive levels of autophagy are low during embryogenesis but are significantly induced after birth and maintain organ function in the postnatal starvation period until a consistent nutrient supply is restored via the maternal milk supply and insulin levels rise. Excessive and long-term induction of autophagy may ultimately lead to destruction of essential proteins and organelles, which beyond a certain threshold results in cell death. The mechanisms that mediate the suppression of autophagy once feeding is established are not known. Furthermore, methods of inhibiting autophagy would be useful to treat or prevent heart failure, myocardial infarction, ischemia reperfusion injury, and diseases of other organs in which autophagy is included in the disease processes of both infants and adults.